Open AccessHepatic Histology in Treatment‐naïve Children With Chronic Hepatitis B Infection Living in the United States and Canada
Author(s) -
RodriguezBaez Norberto,
Murray Karen F.,
Kleiner David E.,
Ling Simon C.,
Rosenthal Philip,
Carlin Kristen,
Cooper Kara,
Schwarz Kathleen B.,
Schwarzenberg Sarah J.,
Teckman Jeffrey H.,
Ghany Marc G.,
Alawad Ahmad Samer
Publication year - 2020
Publication title -
journal of pediatric gastroenterology and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 131
eISSN - 1536-4801
pISSN - 0277-2116
DOI - 10.1097/mpg.0000000000002712
Subject(s) - medicine , fibrosis , cirrhosis , gastroenterology , liver biopsy , inflammation , histology , hepatitis b virus , hepatic fibrosis , hepatitis b , hepatitis c virus , hepatitis , pathology , biopsy , immunology , virus
Objectives: Chronic hepatitis B virus infection is a major cause of morbidity and mortality. The aim of the study is to describe the hepatic histology in children chronically infected with hepatitis B virus living in the United States and Canada. Methods: Liver biopsies of 134 treatment‐naïve children with chronic hepatitis B virus infection were scored for inflammation, fibrosis, and other histological features, and correlated with clinical and laboratory data. Results: Sixty percentage of subjects acquired the infection vertically, 51% were male, and 69% were hepatitis B e antigen‐positive at the time of the biopsy. Hepatitis B DNA levels were generally high (mean 7.70 log IU/mL), as was serum alanine aminotransferase (median 120 U/L). Using the Ishak‐modified histology activity index scoring system, interface hepatitis was mild in 31%, moderate in 61%, and severe in 6%. Lobular inflammation was mild in 54%, moderate in 29%, and marked in 7%. Portal inflammation was mild in 38% and moderate in 62% of subjects. Eighteen percentage had no fibrosis, 59% had portal expansion without bridging fibrosis, 19% had bridging fibrosis, and 4% had cirrhosis. Alanine aminotransferase positively correlated with inflammation and fibrosis. Neither age, duration of infection, nor Hepatitis B virus DNA levels correlated with fibrosis. Fibrosis‐4 index did not correlate with fibrosis but correlated with inflammation. Aspartate aminotransferase/platelet ratio index correlated with both inflammation and fibrosis. Conclusions: Chronic hepatitis B virus infection results in significant inflammation and fibrosis during childhood. Serum alanine aminotransferase is a strong indicator of the severity and extent of hepatic inflammation and fibrosis.